Abstract

Objective To explore the appropriate treatment opportunity and the possible mechanism of ulinastatin combined with bone marrow mesenchymal stem cells (BMSCs) improving sepsis-induced acute lung injury. Methods The cecum end catheter continuous drainage (CASP) was used to establish septic model in 40 male SD rats weighing 180-220 g. The animals were randomly divided into 5 groups (n=8 each group): control (A), septic group (B), ulinastatin combined with BMSCs treatment group at the same time (group C), BMSCs intervention 18 h after administration of ulinastatin (group D), BMSCs intervention 66 h after administration of ulinastatin (group E). The hematoxylin and eosin (HE) staining, immunohistochemistry and Western blotting were applied to examine the lung tissue pathologic changes, and alveolar surface activated protein C and E-calcium expression of mucin respectively. The survival curve was used to expore the survival rate. Results The survival rate among groups had no statistically significant difference (P>0.05). Pathological scores of rat lung tissues in groups A-E were 2.92±0.43, 14.22±1.92, 8.67±1.21, 7.50±1.76 and 10.80±1.47 respectively. The pathological injury of lung tissue in the intervention groups was milder than in group B (P 0.05). Conclusion After immunomodulation, the lung injury caused by sepsis in rats was the mildest within 18 h. The possible mechanism is contributed to the increases in the synthesis of alveolar surface active protein C, and inhibition of the loss of e-cadherin in lung tissue, which can improve the microenvironment of the lung tissue, and delay the lung fibrotic process of sepsis-induced acute lung injury. Key words: Sepsis; Acute lung injury; Pulmonary surfactant protein C; E-Cadherin

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